Research | Bell Lab

Not all breast cancers are equally vulnerable to the immune system, and we believe the answer lies in how tumor cells manage iron. By comparing triple-negative and luminal breast cancers, we're uncovering why some subtypes shut down T cell killing while others remain exposed — a difference that could expand immunotherapy.

Immune checkpoint therapies often fail in colorectal cancer, leaving tumors free to grow unchecked. We're testing whether we can reignite T cells' natural killing power by tipping tumor cells toward an iron-driven death process called ferroptosis.

When a T cell attacks a tumor cell, it triggers the formation of giant internal structures called gigantosomes: a discovery our lab helped describe.. We're now mapping exactly how these structures form and ferry iron to the mitochondria, work that could expose a new tumor vulnerability.

Some tumor cells survive a T cell attack instead of dying: and we study what happens next. These "persister" cells may be seeding cancer recurrence or metastasis, and understanding how they escape death could reveal new ways to enhance T cell killing.

The same molecular process that helps immune cells kill tumors may also drive tissue damage in inflammatory bowel disease. By studying ferroptosis in the gut, we are interested in how to downregulate this killing to prevent autoimmune damage.